Eur J Endocrinol:库欣综合征全血甲基组分析鉴定糖皮质激素相关分子特征

2022-03-13 从医路漫漫 MedSci原创

库欣综合征是一种糖皮质激素过量状态,与糖皮质激素治疗(外源性库欣综合征)或肾上腺皮质激素分泌过多有关。

背景:库欣综合征是一种糖皮质激素过量状态,与糖皮质激素治疗(外源性库欣综合征)或肾上腺皮质激素分泌过多有关。虽然在抑制炎症状态方面有效,但长期使用糖皮质激素与潜在的严重不良反应有关,限制了它们的广泛和长期使用。全身糖皮质激素治疗的临床后果反映在内源性皮质醇过多的状态上。虽然库欣综合征的明显表现很少见,最常与垂体腺瘤有关,但轻度自主皮质醇高分泌更为常见,主要由肾上腺腺瘤引起。库欣综合症与高发病率和高死亡率有关,并通过许多全身症状损害生活质量,包括糖尿病、高血压、骨质疏松症、皮肤瘀伤、肌肉萎缩、神经精神障碍和免疫缺陷。毫无疑问,糖皮质激素过量的持续时间和水平是库欣综合征严重程度的主要决定因素。然而,个体易感性极大地影响每种并发症发生的可能性,并调节其严重程度。在临床的另一边,肾上腺功能不全是一种皮质醇缺乏的状态,导致疲劳和代谢或电解质平衡的急性失代偿,具有潜在的致命后果。肾上腺功能不全可由肾上腺、垂体或下丘脑的结构或功能损害引起,最常见的原因是自身免疫、肿瘤或治疗相关的原因。

目的:库欣综合征是指与糖皮质激素治疗或内源性皮质醇增多症相关的糖皮质激素过多状态。库欣综合征与高发病率有关,具有显著的个体差异。同样,肾上腺功能不全是皮质醇缺乏的一种危及生命的情况。目前,激素检测有助于确定库欣综合征或肾上腺功能不全。然而,没有生物标记物直接量化生物糖皮质激素的作用。本研究的目的是鉴定这些标记。

设计:我们评估了94例来自不同糖皮质激素状态(库欣综合征、优皮素症、肾上腺功能不全)患者的全血DNA甲基组。我们使用了91个样本的独立队列进行验证。

方法:从全血标本中提取白细胞DNA。用Illumina甲基化芯片序列(~85万个CpG位点)测定甲基组。用无监督(主成分分析)和有监督(LIMMA)两种方法探索甲基组图谱。使用套索惩罚回归来选择最优的鉴别特征。

结果:全血甲基化图谱能够根据样本的糖皮质激素状态来区分样本:糖皮质激素过量与DNA低甲基化有关,在库欣综合征纠正后的几个月内恢复。在库欣综合征患者中,FKBP5基因位点存在CpG低甲基化富集现象。糖皮质激素过量的甲基化预测因子建立在一个训练队列上,并在两个独立的队列上得到验证。潜在的CpG位点与特定并发症的风险相关,如糖皮质激素相关性高血压或骨质疏松症,现在需要在独立的队列中确认。

图1糖皮质激素水平对全血DNA甲基化的影响。(A)对整个数据集(n=731 635个CpG站点,n=94个样本)进行基于无监督PCA的两个主成分(PC1,PC2)的样本投影。(B)相对于最易变的CpG位点的全局甲基化(中位数M值)(n=52 727,M值为S.D.)。>0.4)。*P值<0.001,*P值<10−10

图2差异甲基化的CpG位点分布(显性库欣综合征与真皮质疏松症:n=1290)。(A)相对于基因组CpG富集的分布。(B)相对于基因位点结构的分布。(C)基因组分布。以黑色突出显示的CpG位点位于6号染色体上的FKBP5基因位点。

图3库欣综合征样本中FKBP5启动子区甲基化水平。(A)主要队列中与FKBP5基因启动子相关的差异甲基化区域中包括的五个CpG位点的平均甲基化(M值)的盒图表示。(B)ENSAT-HT队列中相同5个CpG位点的甲基化水平的盒图表示。**P值<0.001,*P值<10−5.

图4糖皮质激素过量正常化后甲基组修饰的动力学。对患者P30在库欣综合征纠正前和纠正后三个不同时间点收集的四个样本进行非监督聚类。下面提供了在临床库欣综合征中7426个差异甲基化的CpG位点的平均甲基化(M值)。*P值<10−15

结论:糖皮质激素对全血DNA甲基组有动态影响。这个生物标记物可以帮助更好地评估糖皮质激素的作用。

原文出处:Armignacco R,  Jouinot A,  Bouys L,et al.Identification of glucocorticoid-related molecular signature by whole blood methylome analysis.Eur J Endocrinol 2022 Jan 13;186(2) 

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    2022-03-17 xsybjmu

    学习了

    0

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    2022-03-13 542557560

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    2022-03-13 ms7000001031705413

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